Yang Yong, Guo Xin, Yu Zhi-Cheng, Ma Jia-Qing, Liu Xing-Ling, Li Li-Sha, Xiao Gao-Peng, Liu Xiao-Meng, Li Xin-Nan, Shen Jin-Song, Li Yan-Hua, Liu Rui
Experimental Center of Medical Function, Kunming Medical University, Kunming 650500, China. E-mail:
Nan Fang Yi Ke Da Xue Xue Bao. 2017 Oct 20;37(10):1345-1350. doi: 10.3969/j.issn.1673-4254.2017.10.10.
To elucidate the mechanisms of up regulated expression of cytoplasmic phospholipase A2 (CPLA2) induced by one lung ventilation (OLV) by investigating the interactions between nuclear factor kappaB (NF-κB) and C-PLA2.
Forty-eight healthy Japanese white rabbits were randomized into control group, solvent treatment group (group S), NF-κB inhibitor (PDTC)/solvent treatment group ( group PS), C-PLA2 inhibitor (AACOCF3)/solvent treatment group (group AS), OLV group (group O), solvent treatment plus OLV group (SO group), NFκB inhibitor (PDTC)/solvent treatment plus OLV group (group PSO) and CPLA2 inhibitor (AACOCF3)/solvent treatment plus OLV group (group ASO). ELISA was used to detect arachidonic acid (AA) content in the lung tissues, and NFκB and CPLA2 expressions were detected by Western blotting and quantitative PCR. Lung injuries were assessed based on the lung histological score, and the polymorphonuclear leukocyte count in the bronchial alveolar lavage fluid, myeloperoxidase (MPO) content in the lung tissues, and lung wet/dry weight (W/D) raito were determined.
Treatment of the rabbits with the solvent did not produce any adverse effects. OLV caused obvious lung injury in the rabbits and up regulated the expressions of CPLA2 and NFκB in the lung tissues (P<0.05). In rabbits without OLV, treatment with AACOCF3 or PDTC significantly down regulated both CPLA2 and NFκB expressions without affecting the other parameters. In rabbits with OLV, treatment with AACOCF3 or PDTC obviously lowered CPLA2 and NFκB expressions and lessened the OLV-induced lung injuries.
Both C-PLA2 and NF-κB play important roles and show interactions in OLV-induced lung injury in rabbits.
通过研究核因子κB(NF-κB)与胞质型磷脂酶A2(C-PLA2)之间的相互作用,阐明单肺通气(OLV)诱导的C-PLA2表达上调的机制。
将48只健康的日本白兔随机分为对照组、溶剂处理组(S组)、NF-κB抑制剂(PDTC)/溶剂处理组(PS组)、C-PLA2抑制剂(AACOCF3)/溶剂处理组(AS组)、OLV组(O组)、溶剂处理加OLV组(SO组)、NF-κB抑制剂(PDTC)/溶剂处理加OLV组(PSO组)和C-PLA2抑制剂(AACOCF3)/溶剂处理加OLV组(ASO组)。采用酶联免疫吸附测定(ELISA)法检测肺组织中花生四烯酸(AA)含量,采用蛋白质免疫印迹法和定量聚合酶链反应检测NF-κB和C-PLA2表达。根据肺组织学评分评估肺损伤情况,并测定支气管肺泡灌洗液中多形核白细胞计数、肺组织中髓过氧化物酶(MPO)含量及肺湿/干重(W/D)比值。
用溶剂处理兔子未产生任何不良反应。OLV导致兔子出现明显的肺损伤,并上调肺组织中C-PLA2和NF-κB的表达(P<0.05)。在未进行OLV处理的兔子中,用AACOCF3或PDTC处理可显著下调C-PLA2和NF-κB的表达,而不影响其他参数。在进行OLV处理的兔子中,用AACOCF3或PDTC处理可明显降低C-PLA2和NF-κB的表达,并减轻OLV诱导的肺损伤。
C-PLA2和NF-κB在OLV诱导的兔子肺损伤中均起重要作用,并存在相互作用。